DISSECT THE EFFECTS OF COPZ1 TARGETING: A PROMISING STRATEGY FOR DIFFERENT SOLID TUMORS

We previously identified the coatomer protein complex zeta 1 (COPZ1) as a new putative therapeutic target for thyroid tumors. We classified COPZ1 as an example of NOA (non-oncogene addiction) for thyroid cancer cells: its depletion reduces the in vitro growth of different thyroid tumor cell lines but not for that of normal immortalized thyrocytes; this leads to abortive autophagy, ER stress, unfolded protein response and apoptosis. 

Moreover, COPZ1 depletion induces type I interferon response, which boosts a proinflammatory form of cell death that is able to promote dendritic cell maturation and subsequent T cell response activation. 

The aim of the study is to investigate in an in vivo model the paracrine effects of COPZ1 depletion in thyroid tumor cells, in order to explore the occurrence of an antitumor immune response. The validation of COPZ1 as a therapeutic target in two other solid tumors, prostate and breast cancer, will be also performed.